CLONUS is described as an involuntary rhythmic muscle contraction which accompanies spasticity of ankle muscles, and occurs in people with lesions involving descending motor pathways. Currently, there is a large debate as to the causes of clonus, centering on two different hypotheses. The first proposes the existence of spinal neural oscillators, and the second that oscillation is due to instability of hyperactive stretch reflexes forming a high gain negative feedback regulator. Therefore. the overall objective is to investigate the underlying mechanisms causing clonus. We propose that following a lesion in motor pathways, the excitability of the motoneuron pool increases because of diminished supraspinal or regional inhibitory input, enhancing instability in a marginally stable system. This hypothesis will be tested in four steps. First, a lumped parameter model of the stretch reflex pathway in the human ankle will be developed. Then, systems identification will be done on ankle muscles to determine the properties of the models components. Third, clonus behavior such as oscillation frequency and muscle length change will be measured in pathological subjects, subjected to varying perturbations, and to differing inertial loads. Finally, simulated motoneuron threshold and current frequency relations will be adjusted in the model to examine how the excitability of the motoneuron pool influences the behavior of the ankle reflex. Based on a control systems analysis, we will assess whether these changes promote oscillatory behavior (clonus) in the human ankle reflex.